A nationwide survey of German neurological and neurosurgical departments has found that induced hypertension is used almost universally to manage suspected delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage, despite major uncertainty over how the treatment should be delivered. The study, published in Neurocritical Care, shows that hospitals differ widely in the blood-pressure targets they choose, the monitoring technologies they rely on, the imaging protocols they follow and the point at which they escalate to endovascular treatment. The findings reveal a striking gap between routine clinical practice and the strength of evidence supporting it: a therapy used in nearly every responding center has never been definitively shown in a large randomized trial to improve outcomes.
Aneurysmal subarachnoid hemorrhage occurs when a weakened blood vessel, or aneurysm, ruptures and spills blood into the space surrounding the brain. Although modern procedures can often seal the aneurysm, patients remain vulnerable during the following days to delayed cerebral ischemia, a condition in which parts of the brain receive insufficient blood flow. DCI is one of the main causes of neurological deterioration and long-term disability after the initial hemorrhage. It can result from narrowing of large cerebral arteries, traditionally called vasospasm, but the biology is more complicated. Microvascular dysfunction, impaired autoregulation, disturbances in cerebral perfusion pressure and waves of cortical spreading depolarization can all contribute to an oxygen supply-demand imbalance in brain tissue.
The danger is especially difficult to recognize in patients who are sedated, mechanically ventilated or already neurologically impaired by the original hemorrhage. In those cases, a new weakness, speech disturbance or change in alertness may be impossible to detect through bedside examination. Clinicians therefore combine repeated neurological assessments with physiological monitoring and brain imaging. When DCI is suspected, induced hypertension is often used to raise arterial pressure and increase the pressure gradient driving blood through threatened brain regions. The treatment typically involves an intravenous vasopressor, a drug that constricts blood vessels and raises blood pressure, sometimes combined with fluids or adjustments to other medications. The aim is not simply to produce a higher number on a monitor, but to improve cerebral perfusion while avoiding complications such as cardiac strain, pulmonary edema or further neurological injury.
The German survey was conducted online between May and October 2025 using an 11-item questionnaire sent to 132 departments involved in aneurysmal subarachnoid hemorrhage care. These included 82 neurosurgical and 50 neurological departments. Sixty departments responded, representing 45 percent of those contacted; individual questions had slightly different denominators because incomplete responses were retained for the items that had been answered. Among 59 departments providing data on induced hypertension, 56, or 95 percent, said they used the treatment. Most did so primarily when DCI was suspected rather than as a routine preventive measure: 52 of 59 departments, or 88 percent, reported this approach. The result suggests that clinicians generally reserve blood-pressure augmentation for patients showing signs of threatened cerebral perfusion, even though definitions of “suspected DCI” may vary from one hospital to another.
The most common way of guiding treatment was mean arterial pressure, or MAP, used by 64 percent of responding departments. MAP is an estimate of the average pressure pushing blood through the circulation over a cardiac cycle, and it is often used as a practical surrogate for systemic perfusion. Other departments guided therapy by cerebral perfusion pressure, which accounts for intracranial pressure, or by systolic blood pressure alone. Yet the survey found no consistent national target. Where departments supplied numerical goals, systolic pressure most often fell between 160 and 180 millimeters of mercury, MAP commonly ranged from 90 to 110 millimeters of mercury, and cerebral perfusion pressure targets were generally above 80 millimeters of mercury. These ranges are not interchangeable, because the same systemic pressure can produce different brain perfusion depending on intracranial pressure, vascular resistance and the patient’s own autoregulatory capacity.
Noradrenaline was the dominant drug used to raise blood pressure, reported by 98 percent of departments that provided vasopressor information. The drug can be rapidly adjusted through an infusion and has predictable effects on vascular tone, making it a standard choice in neurocritical care. Dobutamine, which primarily increases cardiac contractility and cardiac output, was used by 37 percent of departments, potentially reflecting concern that inadequate blood flow was related not only to vascular resistance but also to poor cardiac performance. Dopamine and phenylephrine were rarely selected. All departments using induced hypertension relied on vasopressors, while 64 percent also administered fluids. Nearly two-thirds said they would consider reducing the dose of nimodipine, a drug routinely used after subarachnoid hemorrhage to reduce the risk of poor neurological outcome but one that can lower blood pressure. This trade-off illustrates the practical difficulty of treatment: maintaining nimodipine may protect the brain, but hypotension can force clinicians to increase vasopressor exposure or modify therapy.
The survey also showed how hospitals search for evidence of DCI. Transcranial Doppler ultrasonography, which measures blood-flow velocities in major cerebral arteries through the skull, was used by 93 percent of departments. Rising velocities can suggest arterial narrowing, although the technique is operator-dependent and may not reliably capture disturbances in the microcirculation. More specialized monitoring was less widespread. Brain-tissue oxygen measurements were reported by 36 percent of departments, continuous electroencephalography by 13 percent, and cerebral microdialysis by 7 percent. These techniques can provide information about local oxygen availability, electrical activity or metabolic stress, particularly when the neurological examination is unavailable, but they require specialized equipment and expertise.
Computed tomography formed the core of imaging practice. In patients with suspected DCI, 88 percent of departments used CT perfusion, which estimates regional blood flow, blood volume and transit time by tracking contrast material through the brain. CT angiography, used by 79 percent, allowed clinicians to inspect larger cerebral arteries for narrowing or other vascular abnormalities. Noncontrast CT was used by 73 percent, while MRI and MR perfusion were reported by only 9 and 7 percent, respectively. Forty-eight of 56 departments performed imaging in every patient when DCI was suspected, whereas seven mainly restricted imaging to sedated patients and one did not routinely image. Even without suspected DCI, 41 percent performed standardized imaging in all patients and 27 percent did so specifically in sedated patients. Such routine scanning may help detect clinically silent perfusion abnormalities, but the survey cannot show whether it improves outcomes or leads to unnecessary interventions.
When DCI was thought to be developing, 47 percent of departments used induced hypertension alone as their first-line treatment. Another 36 percent combined it with intra-arterial spasmolysis, an endovascular procedure in which a catheter is used to deliver a vasodilating drug directly into constricted cerebral arteries. Nine percent used intra-arterial spasmolysis alone, while 7 percent reported other strategies. The emphasis on combination treatment reflects the fact that DCI is not always caused by a single large artery that can be opened mechanically or pharmacologically. A patient may have visible vasospasm alongside impaired small-vessel flow, disrupted autoregulation or cortical spreading depolarizations, leaving clinicians to address several mechanisms simultaneously. Three-quarters of departments reported having a standard operating procedure for DCI diagnosis and management, but the wide differences in targets and treatment pathways indicate that most protocols remain locally developed rather than nationally standardized.
The evidence gap behind this widespread practice remains substantial. Randomized data are largely limited to the prematurely terminated HIMALAIA trial, while observational studies have produced conflicting results about whether induced hypertension prevents infarction or improves neurological recovery and what complications it may cause. European guidelines have been cautious, with recent recommendations stopping short of an evidence-based endorsement, although expert consensus allows the treatment to be considered when standard measures are insufficient. US guidelines take a more permissive position, stating that individualized blood-pressure elevation may benefit patients with symptomatic DCI while acknowledging the absence of robust randomized evidence. The German survey found that 84 percent of responding departments would participate in a randomized controlled trial, suggesting that clinicians recognize the uncertainty and are willing to test the treatment directly.
The researchers caution that the survey cannot determine whether any blood-pressure target, vasopressor or monitoring strategy is superior. Its moderate response rate may have favored academic centers or hospitals with a particular interest in neurocritical care, potentially exaggerating the use of advanced monitoring and formal protocols. Responses represented departmental practice rather than individual patients, and the questionnaire did not capture treatment duration, vasopressor doses, cardiac monitoring, adverse events, criteria for judging improvement or rules for reducing therapy. Nor did it impose one uniform definition of suspected DCI, meaning that a clinical decline, a Doppler abnormality, a perfusion deficit or an invasive-monitoring change might have triggered treatment in different centers. Still, the central message is clear: induced hypertension has become a near-universal emergency tool in German DCI care, but its practical use is fragmented. Future multicenter trials will need to determine not only whether raising blood pressure helps, but which patients should receive it, what physiological target should guide treatment, how response should be measured and when the potentially risky intervention should be stopped.
